We previously demonstrated that a 6-hydroxydopamine (6-OHDA) induced lesion of substantia nigra (SN), which is a very well known animal model of Parkinson's disease, resulted in memory deficits and increased brain oxidative stress. Also, recent reports had suggested that nicotine from smoke may contribute, at least in some parts, to the apparent neuroprotective effect of tobacco use in Parkinson's disease.
In this way, in the present study we were interested to examine the effects of low-dose nicotine administration (5 days, 0.3 mg/kg/day) in a rat model of Parkinson's disease, on behavioral parameters from Y-maze or shuttle-box task and also on the oxidative stress markers from the temporal lobe, which is one of the most vulnerable cortical area to oxidative stress effects.
The administration of nicotine resulted in significant improvements of short-term memory, as seen in the Y-maze task, as well an increase of conditioned avoidance responses and decreased number of escape failures in the shuttle-box task. Additionally, an increase in the specific activity of glutathione peroxidase and a decrease of the lipid peroxidation processes is reported. Moreover, we found a significant correlation between the behavioral results from the Y-maze and shuttle-box tasks and the levels of oxidative stress markers.
Taken together our data suggest that short-term administration of low-dose nicotine facilitates memory processes and improves the oxidative stress status of the brain, after a 6-OHDA induced lesion of the SN.
"Nicotine is one of the main constituents of tobacco, which can protect neuronal cells against the insults of AD (Yu et al. 2011). Moreover, exposure to nicotine for a short period ameliorated the cognitive performance in AD patients (Ciobica et al. 2012). These findings explained, to some extent, the phenomenon that smokers have a lower incidence of AD. "
[Show abstract][Hide abstract] ABSTRACT: Emerging evidences suggest that nicotine exerts a neuroprotective effect on Alzheimer's disease (AD), yet the precise mechanism is not fully elucidated. Here, HT22 cells were exposed to amyloid beta protein fragment (Aβ)1-42 to mimic the pathological process of neuron in AD. We hypothesized that cannabinoid receptor CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 injury in HT22 cells. CB1 expression in HT22 cells was investigated by immunocytochemistry and Western blot. The injury of HT22 cells was evaluated by cellular morphology, cell viability, and lactate dehydrogenase (LDH) release. The apoptosis of HT22 cells was assessed by flow cytometry and expressions of Bcl-2 and Bax. The results demonstrated that nicotine markedly upregulated CB1 expression, increased cell viability, ameliorated cellular morphology, decreased LDH release, and reduced the apoptotic rate of HT22 cells exposed to Aβ1-42 for 24 h, while the blockade of CB1 or the inhibition of protein kinase C (PKC) partially reversed the neuroprotection. Furthermore, the blockade of CB1 reversed nicotine-induced PKC activation in HT22 cells exposed to Aβ1-42. These results suggest that CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 neurotoxicity, and the neuroprotection may be dependent on the activation of PKC.
"In our previous report, acetylcorynoline impaired the maturation of mouse bone marrowderived dendritic cells via suppression of IkB kinase and mitogenactivated protein kinase activities (Fu et al., 2013).Therefore, acetylcorynoline may also be able to improve inflammation in the brains of patients with PD and reduce DA neuron damage. Some reports have indicated that alkaloids, including caffeine (Sonsalla et al., 2012), nicotine (Ciobica et al., 2012), sinomenine (Qian et al., 2007) and tetrahydroberberine (Wu et al., 2010), have special neuroprotective effects on DA neurons. In addition, isorhynchophylline promotes the degradation of a-synuclein in neuronal cells (Lu et al., 2012). "
[Show abstract][Hide abstract] ABSTRACT: Parkinson's disease (PD), the second most common neurodegenerative disease, impairs motor skills and cognitive function. To date, the drugs used for PD treatment provide only symptomatic relief. The identification of new drugs that show benefit in slowing the decline seen in PD patients is the focus of much current research. Acetylcorynoline is the major alkaloid component derived from Corydalis bungeana, a traditional Chinese medical herb. It has been shown to have anti-inflammatory properties, but no studies have yet described the effects of acetylcorynoline on PD. The aim of this study was to evaluate the potential for acetylcorynoline to improve PD in C. elegans models. In the present study, we used a pharmacological strain (BZ555) that expresses green fluorescent protein specifically in dopaminergic neurons, and a transgenic strain (OW13) that expresses human α-synuclein in muscle cells to study the antiparkinsonian effects of acetylcorynoline. Our experimental data showed that treatment with up to 10 mM acetylcorynoline does not cause toxicity in animals. Acetylcorynoline significantly decreases dopaminergic neuron degeneration induced by 6-hydroxydopamine in BZ555 strain; prevents α-synuclein aggregation; recovers lipid content in OW13 strain; restores food-sensing behavior, and dopamine levels; and prolongs life-span in 6-hydroxydopamine-treated N2 strain, thus showing its potential as a possible antiparkinsonian drug. Acetylcorynoline may exert its effects by decreasing egl-1 expression to suppress apoptosis pathways and by increasing rpn5 expression to enhance the activity of proteasomes.
[Show abstract][Hide abstract] ABSTRACT: Nicotine has been reported to exert certain protective effect in the Parkinson's and Alzheimer's diseases. Whether it has a similar action in focal cerebral ischemia was unclear. In the present study, rats received either an injection of (-)-nicotine hydrogen tartrate salt (1.2 mg/kg, i.p.) or the vehicle 2 h before the 120 min middle cerebral artery occlusion. Neurological deficits and histological injury were assessed at 24 h after reperfusion. The content of endocannabinoids and the expression of cannabinoid receptor CB1 in brain tissues were determined at different time points after nicotine administration. Results showed that nicotine administration ameliorated neurological deficits and reduced infarct volume induced by cerebral ischemia in the rats. The neuroprotective effect was partially reversed by CB1 blockage. The content of the endocannabinoids N-arachidonylethanolamine and 2-arachidonoylglycerol, as well as the expression of cannabinoid receptor CB1 were up-regulated in brain tissues after nicotine delivery. These results suggest that endogenous cannabinoid system is involved in the nicotine-induced neuroprotection against transient focal cerebral ischemia.
Neurochemical Research 11/2012; 38(2). DOI:10.1007/s11064-012-0927-6 · 2.59 Impact Factor
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